Flashcards in Clinical CHF Deck (38):
What 2 formulas must we absolutely know?
1. BP= CO x TPR
2. CO= HR x SV
What dictates the CO?
the filling time (preload), afterload, and inotropism (contractility).
Is the systemic vascular resistance high or low when the CO is low?
the systemic vascular resistance is high
What are the 2 neurohumoral responses that control systemic vascular resistance?
1. sympathetic nervous system
2. renin-angiotensin aldosterone system (RAAS)
What happens to pressure if you increase volume?
you increase pressure also because they are in a direct linear relationship.
What happens if you have too little volume?
you stimulate the RAAS system to retain salt and increase volume and thus pressure.
* The body can overshoot though when it does this.
**What are the 2 types of heart failure?
1. reduced= systolic dysfunction; EF
2. diastolic dysfunction
How do you treat CHF?
find the underlying etiology
What are the etiologies of CHF?
The loss of a critical quantity of functioning myocardial cells after injury to the heart due to:
3. Idiopathic cardiomyopathy
4. Infections (viral myocarditis, Chagas' disease)
5. Toxins (alcohol or cytotoxic drugs)
6. valvular disease
7. prolonged arrhythmias
Where do you begin when a patient comes in?
with the history!
**What are the 4 controlling mechanisms of systolic dysfunction or reduced LV function?
3. inotropism (contractility)
What is the initial treatment for CHF?
to relieve the symptoms
**What is heart failure?
a complex clinical syndrome in which the heart is incapable of maintaining a CO adequate to accommodate metabolic requirements and the venous return.
What is the New York Heart Association (NYHA) classification system for heart failure?
1. SOB with severe exertion
2. SOB with moderate exertion
3. SOB with mild exertion
4. SOB with rest
* you can go from 1 to 2, 2 to 4, 4 to 1...
How does the American College of Cardiology rate heart failure?
A. Have the possibility of developing heart failure because you have risk factors.
B. You're in heart failure and you don't know it (due to compensatory mechanisms: RAAS and sympathetic NS).
C. You're in active heart failure.
D. You have a cardiomyopathy and you will die.
What is the incidence (new cases each year) of heart failure?
What should you think when end systolic or diastolic volume increases?
- neck vein distention
- hepatojugular reflux
- sacral or lower extremity edema
What should you think with pulmonary congestion?
- CO is low
- systemic vascular resistance is up
- cool to the touch distally
What are the symptoms of left ventricular dysfunction?
What are the physical signs of left ventricular dysfunction?
- basilar rales
- pulmonary edema
- S3 gallop
- pleural effusion
What are the 3 compensatory mechanisms of heart failure?
1. Frank-Starling mechanism= increase volume, increase contractility.
2. Neurohormonal Activation= SNS, RAAS, ADH
3. Ventricular remodeling
So what does the body do when we have a decreased MAP?
it will compensate via the sympathetic nervous system (SNS) to increase this by increasing SV, HR, and TPR:
MAP= (HR x SV) x TPR
What are ACE inhibitors and ARBs?
afterload reducers. They inhibit the vasoconstriction and sodium retention that occurs in the kidney during sympathetic stimulation.
*Note: ARBs are NOT inferior to ACE inhibitors
Why do beta blockers PROLONG LIFE?
because they block the sympathetic stimulation on the heart that occurs during heart failure and would lead to myocardial toxicity, increased arrhythmias, and disease progression without them!
What does Vasopressin (ADH) do?
when BP is low, baroreceptors stimulate the hypothalamus to cause the anterior pituitary to release ADH, which travels in the blood to the kidney to cause water retention and vasoconstriction, thus increasing BP.
What are the 3 natriuretic peptides (other neurohormones)?
1. atrial natriuretic peptide (ANP)= on the wall of the atrium and is secreted due to overstretch causing diuretic and vasodilatory properties.
2. brain natriuretic peptide (hBNP)= found in the ventricles and has diuretic and vasodilatory properties.
*Used mostly to gauge progression after a few days. Because this is a marker for heart failure, if it drops, we know we are on the right path.
3. C-type natriuretic peptide (CNP)= predominantly found in the CNS
What are the important endothelium derived relaxing factors (vasodilators)?
What is the endothelium-derived constricting factor?
**How should you approach a class 2 or 3 heart failure patient?
start them on an ACE or ARB and see where they go from there. If their potassium and kidney function are good, but they are still in heart failure, then you can add spirinolactone.
If you use beta blockers, the goal is to get to the highest dose recommended (doesn't always work because the pts BP won't tolerate it). If you can't get to the max dose, you shoot for a goal HR of 60-70.
**Do diuretics prolong life?
NO! They are just used to relieve symptoms. So you use as little of these as possible, and as much of the ACEs, ARBs and beta blockers that you can!
When can you use digoxin?
If you've maxed out on beta blockade and ACEs or ARBs, then if you're still in stage 3 or 4 heart failure, you can add digoxin in SMALL doses.
What can cause digoxin toxicity?
hypovolemia (due to drug level going up as volume goes down), or drugs that compete on the myocardial binding sites with digoxin that put it into the serum.
What is the half-life of digoxin?
Why must we be SOOO careful with digoxin?
because it has a narrow therapeutic index, can cause heart block, or arrhythmias. You will also get yellow vision!
If the pts kidney function is impaired, can you use ACE inhibitor or ARBs?
NO! Instead use long acting nitroglycerin (venodilator) and hydralazine (arterial dilator).
How do you diagnostically evaluate new onset heart failure?
1. determine the type of cardiac dysfunction (systolic vs. diastolic)
2. determine etiology
3. define prognosis
4. guide therapy
What do we do if we've tried all anti-arrhythmic drugs in pts who have reduced LV function (
use a pacemaker= reads and memorizes every beat of your heart! It recognizes the difference between normal beats and ventricular tachycardia. It is programmed at a higher rate than your v-tach, so it will go faster than the v-tach to make the myocardium refractory, preventing the depolarization from going through! If your heart doesn't beat in over 8 seconds, it will defibrillate you, and it feels like you were kicked in the chest by a horse!